Tinnitus is the perception of sound in the absence of corresponding external sounds. Tinnitus may be caused by injury, infection or the repeated bombast of loud sound, and can appear in one or both ears. Although known for its high-pitched ringing, tinnitus is an internal noise that varies in its pitch and frequency. The sound perceived may range from a quiet background noise to a signal loud enough to drown out all outside sounds.
Tinnitus affects approximately 50 million Americans or about 15% of the general population. There is no effective treatment to ameliorate tinnitus. The prior art has included devices and methods that attempt to mask tinnitus.
General Hearing and several others manufacture an earpiece that can generate sound. The masking methods work well for people who suffer mild forms of tinnitus but don't work for people who suffer from loud tinnitus because to mask the tinnitus, the external sound has to be louder than the tinnitus.
Some treatments, such as drugs, surgery, psychotherapy and masking, exist, but none are consistently effective and may have significant side effects. Here we propose to use sound to suppress tinnitus. Different from previous masking methods, which use an external sound that is typically louder than the tinnitus and has similar pitch quality to the tinnitus, we propose to use optimized sounds that may be softer and have different pitch qualities than the tinnitus. Another significant difference between previous masking devices and the present suppressing method is that the masking effect is instantaneous, while the present suppressing method usually takes time to develop and decay. The sound can be delivered either acoustically via an audio device (e.g., MP3 players, iPod® devices, or other ear devices) or electrically via a temporary or permanent implant.
In particular, various medications have been used to treat tinnitus, which are aimed at the disease or its co-morbidities. Tinnitus is often associated with anxiety and depression. Whether the condition causes psychological distress or whether tinnitus is more prevalent in people with psychological disorders is under debate. It has been suggested that tricycilc antidepressants treat the underlying psychological problems rather than the tinnitus directly. Some studies have demonstrated significant decrease in tinnitus intensity with the administration of intravenous (IV) lidocaine but have not reproduced the effect with oral analogues such as tocainide. IV administration of lidocaine is not a practical method due to its short half-life and serious side effects. Other agents, such as carbamazepine, alprazolam, baclofen, betahistine, and cinnarizine have also been studied as possible tinnitus treatments, with inconsistent results. Selective serotonin reuptake inhibitors have shown no benefit or a slight benefit in placebo-controlled studies.
Tinnitus masking devices of the prior art deliver a continuous low-level noise or tone to the ear that results in camouflaging of the tinnitus. Use of the device has been shown to reduce tinnitus severity. The Neuromonics tinnitus treatment is a new method of acoustic stimulation in combination with a structured program of counseling. The device output is a broadband stimulus that is constructed for each individual's hearing profile. Three clinical trials reported general improvement in quality of life of patients using this treatment. Hearing aids also grant partial or total relief from tinnitus by amplifying external sound stimuli thereby decreasing the awareness of the presence of tinnitus. Hearing aids are usually tried as first line treatment in patients with tinnitus in the presence of hearing loss. Hearing aids can also be used in combination with sound generators that increase the rate of success.
In the end of 1980s the neurophysiological model of tinnitus was proposed which then elicited the development of a new therapeutic approach called tinnitus retraining therapy (TRT). TRT consists of counseling along with delivery of a low-level, constant white noise to the affected ear(s) of a patient. The sound usually results in habituation of the patient's auditory system to the tinnitus thereby decreasing the patient's awareness of their condition. The rate of success varies between different patients. TRT requires one-to-two years of therapy for effective management of tinnitus.
Cochlear implantation has been found to be effective in reducing tinnitus in 28% to 79% of patients who have associated bilateral severe sensorineural hearing loss in previous studies. Exacerbation of tinnitus is reported in 9% of patients after cochlear implantation. Success with cochlear implants in decreasing tinnitus has led to other forms of electric stimulation, including transtympanic stimulation of the cochlea, vestibulocochlear nerve stimulation, and transcranial magnetic stimulation of the auditory cortex. Recent studies have shown that 1 out of 3 cochlear implant users and 5 out of 11 (45%) transtympanic subjects showed substantial or total tinnitus relief while stimulated by high rate pulse trains. More than that, the external perception was either presented subthreshold or diminished to below threshold within a short period of time. This is the ideal situation for tinnitus suffers since both the tinnitus and external stimulus are not perceived as a result. In a review of the literature, unilateral cochlear implant use was suggested to be associated with decline of contralateral tinnitus in 67% of patients. The effect of a cochlear implant is demonstrated to be due to masking of tinnitus by surrounding sounds that are newly perceived or from electrical stimulation of the auditory nerve. The mechanisms underlying the complexity of tinnitus are unclear, and a cure for this condition remains elusive. The prevailing theories generally point to either a central or peripheral source of subjective tinnitus, defined as sound perceivable only to the patient without a clear organic cause. The reality most likely involves a combination of both, with peripheral injuries and pathology causing functional and architectural changes in the central nervous system.
United States Patent Application Publication 2007/0203536 (Hochmair et al.) describes cochlear implant devices as well as other implantable devices useable to deliver tinnitus treatment. The entire disclosure of United States Patent Application Publication 2007/0203536 is expressly incorporated herein by reference.
U.S. Pat. No. 7,347,827 (Choy) describes monofrequency tinnitus patient treatment apparatus and process wherein phase cancellation effects are purported to be achieved by utilizing an externally generated sound which is subjectively selected by the monofrequency tinnitus patient to match in both tone and loudness his or her tinnitus sound. This subjectively selected externally generated sound wave which matches in tone and loudness the patient's tinnitus sound, is either (i) sequentially phase shifted through a plurality of phase shift sequence steps totaling at least 180 degrees or (ii) alternatively is directly phase shifted in essentially a single step motion into a 180 degree, out-of-phase reciprocal, canceling relationship with the patient determined tinnitus tone. The sequential steps of the phase shifted tone or the directly phase shifted tone are applied to the tinnitus patient to effect cancellation or diminishment of the patient's tinnitus. The entire disclosure of U.S. Pat. No. 7,347,827 (Choy) is expressly incorporated herein by reference.
Phase cancellation techniques, such as that described in U.S. Pat. No. 7,347,827 (Choy) may not be optimally effective in treating tinnitus. Most tinnitus is of high frequency (>1000 Hz) although some low-frequency tinnitus cases do exist. However, even if a person's tinnitus is low frequency, the phase canceling techniques may be ineffective or less than optimal because the perceived tinnitus sound is a neural impulse not an acoustic sound and cannot be physically or externally cancelled by phase inversion. Physiologically all sounds will be half-wave rectified in the cochlea and become digital-like pulses (called action potentials) in the nervous system. An out-of-phase external sound will add, rather than cancel, the internally-generated tinnitus.
Tinnitus occurs in the setting of sensorineural hearing loss in the majority of patients, thus the postulate that tinnitus originates peripherally in the cochlea. Noise damage causes molecular changes to structural proteins in stereocilia and the cuticular plate. Cytoplasmic calcium levels increase dramatically in response to sound, potentially disrupting normal hair cell function. Progressive insult results in complete destruction of hair cells in certain regions of the basilar membrane. Aberrant auditory signals occur around areas of hair cell loss, an edge effect that results in the perception of sound. Furthermore, auditory nerve fibers are spontaneously active during quiet, resulting in neurotransmitter release. Loss of the spontaneous activity can lead to abnormal central auditory activity, which could be perceived as sound. Lack of sound input and edge effects as a cause of tinnitus could explain the reduction of tinnitus commonly seen following cochlear implantation. Tinnitus suppression by electrical stimulation in hearing and deaf patients has been shown in a relatively recent study.
On the other hand, not all patients with hearing loss experience tinnitus, and not all tinnitus patients have hearing loss. Sectioning of the auditory nerve can result in tinnitus, suggesting a central etiology. Positron emission tomography (PET) imaging of patients with tinnitus shows unilateral neural activity in Brodmann areas 21,22, and possibly 42. These effects were decreased with lidocaine administration, a known suppressor of tinnitus. Sounds caused bilateral activity regardless of which ear was stimulated. Patients who experienced tinnitus in response to facial movement showed unilateral changes in cerebral blood flow. Another study using single photon emission computed tomography (SPECT) imaging during tinnitus showed a 16% increase in signal in the right auditory cortex and a 5% increase in the left, whereas noise caused bilateral change. The effect was eliminated by lidocaine administration. This difference in the activation pattern supports a theory of central generation of tinnitus.
This interpretation is consistent with animal models of tinnitus showing changes in spontaneous activity of the dorsal cochlear nucleus (DCN) following noise or cisplatin exposure. This hyperactivity persists following ablation of the damaged cochlea, suggesting that while a peripheral injury may stimulate a change in the DCN, the central hyperactivity is independent of peripheral input.
Tinnitus has been separated in three categories depending on severity and if hearing loss is present. Category 0 is characterized by the tinnitus having a low impact on the person's life. Categories 1 and 2 are used to describe tinnitus with a high impact on life with Category 2 indicating the presence of subjective hearing loss that accompanies the tinnitus. For our studies this convention was followed but a second parameter based on loudness was defined. The loudness parameter was determined by each subject as Low. Moderate or High. On a 10-point scale with 1 being the lowest sound (threshold) and 10 being the upper limit of loudness, Low is 0 to 3. Moderate is 3 to 6, and High is 6 to 10. Careful measures were taken to ensure each subject understands they are ranking loudness and not annoyance.
FIG. 1 of this patent application is a graphic representation of tinnitus severity classification and the typical tinnitus patient population. Patients within category 0 are least likely to seek tinnitus treatment. Category 1 and 2 patients with low levels of loudness are likely to be helped by TRT. It has been shown that TRT helps in relaxation for a majority of patients (72.5%) but benefits a much smaller percentage with respect to their ability to work (25.5%) and sleep (47%). At present, category 1 and 2 patients with high levels of loudness are often left without effective treatment.
There remains a need in the art for the development of new devices and methods for the treatment of tinnitus.